Joint homografts fail because of a delayed immune response to the cartilage. It is proposed to show that the synovium is responsible for joint homograft rejection. Osteochondral grafts of the distal dog femur with 5 mm. of subchondral bone will be transplanted into recipient dogs without destroying the ligaments, and fixed securely with a compression screw, eliminating post operative plaster immobilization. The antigenic determinants of the cartilage reside in the proteoglycan (P-G) component of the matrix. Cartilage antigen is concentrated in the synovial cells creating an antigen-antibody reaction in that tissue. This results in a hypertrophic synovium which forms a pannus with release of lysozomal enzymes and destroys the articular cartilage in a manner similar to that seen in rheumatoid arthritis. The presence of proteoglycan antigen in synovium and cartilage will be sought by layering these tissues with rabbit anti-dog P-G serum using immunofluorescent techniques. P-G bound globulin will be demonstrated by layering synovium and cartilage with sheep anti-dog gamma globulin also using immunofluorescent techniques. Detection of delayed hypersensitivity will be studied using intradermal skin and lymphocyte inhibition tests. Should these methods show that the synovium is responsible for homograft rejection transplantation will be done in conjunction with synovectomy and immuno suppressive drugs.